Tislelizumab in Combination with Chidamide, Prednisone, Etoposide, and Lenalidomide Followed By Autologous Stem Cell Transplant in Patients with Relapsed or Refractory Hodgkin Lymphoma

Background

Approximately 10% to 30% of Hodgkin lymphoma (HL) patients suffer primary refractory or disease relapse (R/R). Our objective is to assess the efficacy and safety of tislelizumab in combination with chidamide, prednisone, etoposide, and lenalidomide (T-CPEL) as an introductory treatment following autologous hematopoietic stem cell transplantation (ASCT) or tislelizumab combined with bendamustine (TB) as consolidation in R/R HL.

Methods

Patients with R/R classic HL (cHL) who received T-CPEL regimen were included in our retrospective cohort study.

Results

Between January 2020 and December 2022, a total of 11 patients with R/R cHL were enrolled in our project. The average number of previous systemic therapies was 2 (range 1-6). All patients received at least four cycles of the T-CPEL regimen as an introductory treatment. There was an overall response rate (ORR) of 90.9%, with a complete remission (CR) rate of 36.4%. Five eligible patients underwent ASCT after receiving TB, while six ineligible patients only received TB consolidation therapy. The median follow-up was 21.6 months, and the expected three-year progression free survival (PFS) and overall survival (OS) rate were estimated to be 81.8% and 100.0%, respectively. During the introduction regimen of T-CPEL, 14 adverse events were recorded, most of which were grade one or grade two. No treatment‐related deaths or discontinuation occurred.

Conclusion

The salvage therapy consisting of tislelizumab plus CPEL demonstrated both effectiveness and tolerability in treating R/R cHL cases. Furthermore, following ASCT or TB therapy, there was an increased likelihood for achieving a cure.

No relevant conflicts of interest to declare.

Lenalidomide, as an immunomodulatory drug, exhibits a wide range of action including the promotion of programmed cell death in malignant cells, inhibition of angiogenesis, and stimulation of NK cells and T-cells to indirectly modify the tumor microenvironment. In cHL, the microenvironment, where the Hodgkin/Reed-Sternberg cells-nurtured, plays a vital role in creating a biological habitat that surports their survival while hindering immune detection. Histone deacetylase (HDAC) plays a critical role in various essential cellular functions, including cell cycle progression, angiogenesis, cell differentiation, programmed cell death, and immunity. Consequently, HDAC inhibitors (HDACi) have emerged as potential antitumor therapies for many hematologic and solid neoplasms.